Initial exposure to a severe stressor can result in diminished pain reflexes. Repeated exposures result in a progressive decline of the analgesic response, in much the same manner that the pituitary-adrenal responses to stress show adaptation. However, not all stressors induce analgesia, including some that produce maximal elevations in plasma levels of beta-endorphin, ACTH and adrenal corticosteroids. Some stressors induce an analgesia that is sensitive to opiate receptor blockade by naloxone, others cause a non-naloxone sensitive analgesia. The proposed set of psychophysical experiments will assess whether the sensory changes induced by various stressors in rats are specific to the modality of pain or whether they are accompanied by deficits in auditory and/or visual acuity as well. Sensory thresholds will be measured by a recently developed psychophysical technique, based upon the modulation of the startle response by weak stimuli that precede the startle-eliciting stimulus. This reflex inhibition procedure will circumvent the confounding effects of stress upon the performance aspects of traditional operant sensory discrimination techniques. An interlocking set of experiments will also determine whether opioid and non-opioid forms of stress-induced analgesia differ in their sensory correlates and, consequently, whether either or both reflects a true analgesic state. In turn these data will bear on whether the diverse physiological properties exhibited by current examples of stress-induced analgesia may be counted as evidence for the existence of more than one intrinsic pain-inhibitory system.